Can diabetic nephropathy patients eat kelp?

Written by Zhou Qi
Nephrology
Updated on April 23, 2025
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Patients with diabetic nephropathy should avoid eating seafood, including various types of sea fish, shellfish, as well as seaweed, kelp, and so on. This is because these seafood products contain a certain amount of purines, and some foods have a high purine content. When purines enter the human body, they are metabolized and eventually converted into uric acid, which needs to be excreted by the kidneys. Patients with kidney disease have decreased ability to excrete uric acid, and the accumulation of uric acid may cause further damage to the kidneys and also affect the cardiovascular and cerebrovascular systems. Therefore, generally speaking, it is advised that patients with diabetic nephropathy should avoid eating kelp. However, if the patient’s condition is in the early stages and kidney function is still normal, consuming some kelp in moderation generally should not be a problem, but it should not be consumed in large amounts.

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Written by Zhou Qi
Nephrology
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Can diabetic nephropathy cause blood in urine?

Generally speaking, diabetic nephropathy does not cause hematuria. The main site of damage in diabetic nephropathy is indeed the glomerulus. Prolonged hyperglycemia and metabolic disorders can lead to damage to the capillaries of the glomerulus. However, the main clinical characteristic of this damage is proteinuria, which causes glomerulosclerosis and may also lead to renal failure, but it is rare for patients to have red blood cells in their urine or to experience hematuria. Therefore, if a patient with diabetic nephropathy has visible hematuria, such as red or tea-colored urine, it is necessary to check for other causes beyond diabetes, such as urinary tract infections, urogenital system stones, tumors, etc., all of which can cause hematuria.

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Nephrology
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Does diabetic nephropathy cause back pain?

Diabetic nephropathy generally does not cause symptoms of back pain. Diabetic nephropathy refers to patients with long-term hyperglycemia, typically those whose blood sugar has been elevated for ten years or more, causing damage to the small blood vessels. The kidneys, being rich in small blood vessels, undergo glomerular sclerosis. Early in the disease, patients experience an increased glomerular filtration rate. As the condition progresses, proteinuria gradually increases. When proteinuria occurs, patients may exhibit noticeable edema, and in some cases, patients may develop severe edema due to substantial proteinuria, leading to serious complications like pulmonary edema and heart failure, which manifest as respiratory difficulties and chest tightness. However, these conditions do not cause back pain, even though there is glomerular sclerosis, as patients do not feel any pain associated with it.

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Nephrology
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Is stage three diabetic nephropathy severe?

Stage three of diabetic nephropathy refers to patients who have persistent microalbuminuria, indicating a relatively mild state of the disease at this time. In fact, diabetic nephropathy is divided into five stages. During the first and second stages, patients generally do not exhibit specific symptoms clinically and may even test negative for proteinuria; however, an increase in kidney size and glomerular filtration rate may occur. By the third stage, patients begin to exhibit small or micro amounts of urinary albumin. The pathological damage to the kidneys at this stage is not considered particularly severe. Patients may experience hyalinization of small arteries and nodular lesions in the glomeruli. Within the staging of diabetic nephropathy, this does not constitute a particularly severe phase; however, the condition of the patients may continue to progress, leading to significant proteinuria and even renal failure.

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How to check for diabetic nephropathy?

For the examination of diabetic nephropathy, patients first need to undergo routine urinalysis and check for the urinary albumin excretion rate. Generally speaking, one characteristic of diabetic nephropathy is the presence of urinary protein. A urinary albumin excretion rate between 20 and 200 µg/min is an important basis for diagnosing early diabetic nephropathy. If a patient’s urinary albumin excretion rate consistently exceeds 200 µg/min, significant diabetic nephropathy is often considered. Of course, this is under the assumption that the patient has had diabetes for at least ten years and has diabetic retinopathy. A kidney biopsy is needed for confirmation. Of course, to assess the impact of diabetic nephropathy on kidney function, blood tests for serum creatinine and urea nitrogen are necessary.

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Is diabetic nephropathy stage 3 reversible?

Patients with diabetic nephropathy actually have an irreversible condition. If a patient has developed mild to moderate proteinuria and entered stage three, it's generally because of long-term high blood sugar, oxidative stress, and an excess of glycation end products damaging the capillaries of the glomerulus, resulting in increased permeability and the occurrence of proteinuria. The damage that has already occurred cannot be reversed; however, patients still need active treatment to control their blood sugar and blood pressure in order to slow down the progression of diabetic nephropathy as much as possible. Stage three diabetic nephropathy is incurable, but treatment can slow the progression of the kidney disease, preventing the development from microalbuminuria to macroalbuminuria. Stage three refers to the early period of diabetic nephropathy, typically seen in diabetic patients who have had the disease for more than five years. It can feature a continuous increase in urinary albumin excretion rates. High filtration rates and long-term poor metabolic control may be reasons for the persistent microalbuminuria. During this stage, patients may experience a mild increase in blood pressure, and reducing blood pressure can decrease the excretion of microalbumin. During this period, strict control of blood sugar is necessary. Oral hypoglycemic drugs can be used for treatment, and it's crucial to regularly monitor fasting blood glucose, postprandial blood glucose, and glycated hemoglobin. Blood pressure should also be actively controlled, generally targeting a value of 130/80mmHg. Angiotensin-converting enzyme inhibitors and angiotensin II receptor antagonists are preferred as they can lower blood pressure, reduce proteinuria, and have a protective effect on the kidneys, thus delaying the progression of kidney disease.